Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/49500
Campo DC Valoridioma
dc.contributor.authorEmbade, N.en_US
dc.contributor.authorValeron, P. F.en_US
dc.contributor.authorAznar, S.en_US
dc.contributor.authorLopez-Collazo, E.en_US
dc.contributor.authorLacal, J. C.en_US
dc.date.accessioned2018-11-24T08:07:03Z-
dc.date.available2018-11-24T08:07:03Z-
dc.date.issued2000en_US
dc.identifier.issn1059-1524en_US
dc.identifier.urihttp://hdl.handle.net/10553/49500-
dc.description.abstractRho proteins, members of the Ras superfamily of GTPases, are critical elements in signal transduction pathways governing cell proliferation and cell death. Different members of the family of human Rho GTPases, including RhoA, RhoC, and Rac1, participate in the regulation of apoptosis in response to cytokines and serum deprivation in different cell systems. Here, we have characterized the mechanism of apoptosis induced by Rac1 in NIH 3T3 cells. It requires protein synthesis and caspase-3 activity, but it is independent of the release of cytochrome c from mitochondria. Moreover, an increase in mitochondria membrane potential and the production of reactive oxygen species was observed. Rac1-induced apoptosis was related to the simultaneous increase in ceramide production and synthesis of FasL. Generation of FasL may be mediated by transcriptional regulation involving both c-Jun amino terminal kinase as well as nuclear factor-κB-dependent signals. None of these signals, ceramides or FasL, was sufficient to induce apoptosis in the parental cell line, NIH 3T3 cells. However, any of them was sufficient to induce apoptosis in the Rac1-expressing cells. Finally, inhibition of FasL signaling drastically reduced apoptosis by Rac1. Thus, Rac1 seems to induce apoptosis by a complex mechanism involving the generation of ceramides and the de novo synthesis of FasL. These results suggest that apoptosis mediated by Rac1 results from a signaling mechanism that involves biochemical and transcriptional events under control of Rac1.en_US
dc.languageengen_US
dc.relation.ispartofMolecular Biology of the Cellen_US
dc.sourceMolecular Biology of the Cell[ISSN 1059-1524],v. 11(12), p. 4347-4358 (Diciembre 2000)en_US
dc.subject32 Ciencias médicasen_US
dc.subject2407 Biología celularen_US
dc.subject.otherApoptosisen_US
dc.subject.otherGTAPasesen_US
dc.subject.otherCeramidesen_US
dc.titleApoptosis induced by Rac GTPase correlates with induction of FasL and ceramides productionen_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1091/mbc.11.12.4347en_US
dc.identifier.scopus0033636641-
dc.contributor.authorscopusid57195579521-
dc.contributor.authorscopusid6603469417-
dc.contributor.authorscopusid8702853600-
dc.contributor.authorscopusid8775488800-
dc.contributor.authorscopusid7004811766-
dc.description.lastpage4358en_US
dc.description.firstpage4347en_US
dc.relation.volume11en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.description.numberofpages12en_US
dc.utils.revisionen_US
dc.date.coverdateDiciembre 2000en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.jcr8,482-
dc.description.jcrqQ1-
dc.description.scieSCIE-
item.grantfulltextnone-
item.fulltextSin texto completo-
crisitem.author.deptGIR IUIBS: Medio Ambiente y Salud-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología-
crisitem.author.orcid0000-0001-5865-7003-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameFernández Valerón, Josefa Pilar-
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